中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2008年
48期
3432-3435
,共4页
夏尊恩%李艳%汪明%吴青
夏尊恩%李豔%汪明%吳青
하존은%리염%왕명%오청
E选择素%有丝分裂素激活蛋白激酶类%CD40配体%人脐静脉内皮细胞%阿托伐他汀
E選擇素%有絲分裂素激活蛋白激酶類%CD40配體%人臍靜脈內皮細胞%阿託伐他汀
E선택소%유사분렬소격활단백격매류%CD40배체%인제정맥내피세포%아탁벌타정
E-selectin%Mitogen-activated protein kinases%CD40 ligand%Human umbilicalvein endothelial cells%Atorvastatin
目的 探讨阿托伐他汀对CD40L诱导人脐静脉内皮细胞(HUVEC)表达E-选择素的影响及其信号转导通路的关系.方法 原代培养HUVEC,给予CD40L刺激和不同浓度阿托伐他汀干预.应用反转录聚合酶链反应(RT-PCR)和流式细胞术分别检测阿托伐他汀对CD40L诱导的HUVEC的E-选择素mRNA和细胞表面E-选择素表达情况.同时通过蛋白印迹法检测细胞外信号调节激酶(ERK1/2)蛋白磷酸化的表达.结果 0.1、1、10μmol/L阿托伐他汀可浓度依赖性下调CD40L诱导的HUVEC E-选择素mRNA及蛋白的表达.1 μmol/L阿托伐他汀可使E-选择素蛋白下调48.68%,10μmol/L阿托伐他汀可使E-选择素蛋白下调70.25%.同时不同浓度阿托伐他汀均能抑制CIM0L诱导的ERK1/2磷酸化水平,其表达分别下凋至CD40L刺激组的81%±6%、73%±5%和41%±5%.结论 阿托伐他汀能通过ERK1/2信号转导通路抑制CD4OL诱导的内皮细胞E-选择素表达.
目的 探討阿託伐他汀對CD40L誘導人臍靜脈內皮細胞(HUVEC)錶達E-選擇素的影響及其信號轉導通路的關繫.方法 原代培養HUVEC,給予CD40L刺激和不同濃度阿託伐他汀榦預.應用反轉錄聚閤酶鏈反應(RT-PCR)和流式細胞術分彆檢測阿託伐他汀對CD40L誘導的HUVEC的E-選擇素mRNA和細胞錶麵E-選擇素錶達情況.同時通過蛋白印跡法檢測細胞外信號調節激酶(ERK1/2)蛋白燐痠化的錶達.結果 0.1、1、10μmol/L阿託伐他汀可濃度依賴性下調CD40L誘導的HUVEC E-選擇素mRNA及蛋白的錶達.1 μmol/L阿託伐他汀可使E-選擇素蛋白下調48.68%,10μmol/L阿託伐他汀可使E-選擇素蛋白下調70.25%.同時不同濃度阿託伐他汀均能抑製CIM0L誘導的ERK1/2燐痠化水平,其錶達分彆下凋至CD40L刺激組的81%±6%、73%±5%和41%±5%.結論 阿託伐他汀能通過ERK1/2信號轉導通路抑製CD4OL誘導的內皮細胞E-選擇素錶達.
목적 탐토아탁벌타정대CD40L유도인제정맥내피세포(HUVEC)표체E-선택소적영향급기신호전도통로적관계.방법 원대배양HUVEC,급여CD40L자격화불동농도아탁벌타정간예.응용반전록취합매련반응(RT-PCR)화류식세포술분별검측아탁벌타정대CD40L유도적HUVEC적E-선택소mRNA화세포표면E-선택소표체정황.동시통과단백인적법검측세포외신호조절격매(ERK1/2)단백린산화적표체.결과 0.1、1、10μmol/L아탁벌타정가농도의뢰성하조CD40L유도적HUVEC E-선택소mRNA급단백적표체.1 μmol/L아탁벌타정가사E-선택소단백하조48.68%,10μmol/L아탁벌타정가사E-선택소단백하조70.25%.동시불동농도아탁벌타정균능억제CIM0L유도적ERK1/2린산화수평,기표체분별하조지CD40L자격조적81%±6%、73%±5%화41%±5%.결론 아탁벌타정능통과ERK1/2신호전도통로억제CD4OL유도적내피세포E-선택소표체.
Objective To investigate the regulatory effects of atorvastatin on CD40L induced E-selectin expression in endothelial cells and the association thereof with signal pathway.Methods Human umbilical vein endothelial cells (HUVECs) were obtained from umbilical cord newly delivered and incubated with CD40L for 24 hours with or without pretreated by atorvastatin of the concentrations of 0.1, 1, or 10 μmol/L.The protein and mRNA levels of E-selectin were detected by flow cytometry and reverse transcription polymerase chain reaction (RT-PCR) respectively.The extracellular signal regulated kinase (ERK) 1/2 activation was analyzed by Western blotting.Results The E-selectin mRNA expression level of the HUVECs treated by atorvastatin was lower than that of the CD40I.stimulation group by 33.33% when the atorvastatin concentration was 1 μmol/L, and was lower by 45.16% when the atorvastatin concentration was 10 μmol/L.The E-selectin protein expression level of the HUVECs treated by atorvastatin was lower than that of the CD40L stimulation group by 48.68% when the atorvastatin concentration was 1 μmol/L, and was lower by 70.25% when the atorvastatin concentration was 10 μmol/L.The phosphorylation level of ERK1/2 was enhanced by CD401.stimulation and the CD40L induced phosphorylation of ERK1/2 decreased by 81% ± 6% ,73% ± 5%, and 41% ± 5% respectively after atorvastatin stimulation.Conclusion Atorvastatin decreases the CD40L induced E-selectin expression in endothelial cells while atorvastatin at 0.1 - 10 μmol/L concentration-dependently through inhibiting the activation of ERK1/2.
